Previous studies have employed the carrageenan guinea pig model for ulcerative colitis to determine whether bacteria play a role in the experimental disease. Antimicrobial trials, and microflora simplification studies have yielded a single strain of Bacteroides vulgatus from carrageenan treated conventional guinea pigs which can promote ulcerations in gnotobiotic animals with or without carrageenan treatment. It has also been shown that stool from human ulcerative colitis patients, guinea pigs with experimental colitis and B. vulgatus associated gnotobiotes contain chemotactic activity, CPE and LCFFA not detected in healthy animal cecal content or stool from patients with other inflammatory bowel diseases. The goals of the present research are to 1) deterine whether B. vulgatus, a normal constituent of the human intestinal microflora, has strain specific characteristics which promote large bowel inflammation, 2) to determine whether a specific bacterial cell componant is responsible for inflammation and 3) to test possible mediators of inflammation as causal factors in the experimental disease. The techniques employed will include in vitro CPE assays using Vero cell, LCFFA determinations using GLC, cecal organ culture for prostaglandin measurements by RIA and chemotaxis assays to screen B. vulgatus strains and cell componants isolated from various sources to determine whether strain differences in biolgoic activity occur. In vivo assay of B. vulgatus strains for their ability to promote cecal ulcerations will employ the carrageenan model and gnotobiotic guinea pigs. The overall objectives of this research are to gain a better understanding of the role bacteria play in the experimental disease and to relate these findings to the human disease process.